Clinicopathological features of Churg-Strauss syndrome-associated neuropathy. (1/216)We assessed the clinicopathological features of 28 patients with peripheral neuropathy associated with Churg-Strauss syndrome. Initial symptoms attributable to neuropathy were acute painful dysaesthesiae and oedema in the dysaesthetic portion of the distal limbs. Sensory and motor involvement mostly showed a pattern of mononeuritis multiplex in the initial phase, progressing into asymmetrical polyneuropathy, restricted to the limbs. Parallel loss of myelinated and unmyelinated fibres due to axonal degeneration was evident as decreased or absent amplitudes of sensory nerve action potentials and compound muscle action potentials, indicating acute massive axonal loss. Epineurial necrotizing vasculitis was seen in 54% of cases; infiltrates consisted mainly of CD8-positive suppressor/cytotoxic and CD4-positive helper T lymphocytes. Eosinophils were present in infiltrates, but in smaller numbers than lymphocytes. CD20-positive B lymphocytes were seen only occasionally. Deposits of IgG, C3d, IgE and major basic protein were scarce. The mean follow-up period was 4.2 years, with a range of 8 months to 10 years. Fatal outcome was seen only in a single patient, indicating a good survival rate. The patients who responded well to the initial corticosteroid therapy within 4 weeks regained self-controlled functional status in longterm follow-up (modified Rankin score was < or = 2), while those not responding well to the initial corticosteroid therapy led a dependent existence (P < 0.01). In addition the patients with poor functional outcomes had significantly more systemic organ damage caused by vasculitis (P < 0.05). Necrotizing vasculitis mediated by cytotoxic T cells, leading to ischaemic changes, appears to be a major cause of Churg-Strauss syndrome-associated neuropathy. The initial clinical course and the extent of systemic vasculitic lesions may influence the long-term functional prognosis. (+info)
Pulmonary eosinophilia associated with montelukast. (2/216)Antileukotriene drugs are new therapeutic agents that have recently been approved for the treatment of asthma. Several cases of eosinophilic conditions including Churg-Strauss syndrome have been reported to be associated with zafirlukast, a cysteinyl leukotriene type 1 receptor antagonist. So far no other leukotriene modifier has been associated with the syndrome. The case history is presented of a man with allergic rhinitis and asthma who had received intermittent pulse therapy with oral corticosteroids. Pulmonary eosinophilia developed while he was receiving treatment with montelukast, a chemically distinct cysteinyl leukotriene type 1 receptor antagonist. After discontinuation of montelukast therapy and administration of systemic corticosteroids the patient's symptoms reversed rapidly and there was prompt resolution of the pulmonary infiltrates. We believe that cysteinyl leukotriene type 1 receptor antagonists are safe and effective drugs for most patients with asthma but caution is needed for those with more severe disease who require systemic corticosteroids, especially if they show characteristics of the atypical allergic diathesis seen in the prodromal phase of Churg-Strauss syndrome. (+info)
No association between neutrophil FcgammaRIIa allelic polymorphism and anti-neutrophil cytoplasmic antibody (ANCA)-positive systemic vasculitis. (3/216)ANCA, implicated as having a pathogenic role in systemic vasculitis, can activate tumour necrosis factor-alpha (TNF-alpha)-primed neutrophils by cross-linking surface-expressed ANCA antigens with neutrophil FcgammaRIIa receptors to release reactive oxygen species. The FcgammaRIIa receptor exists as polymorphic variants, R131 and H131, which differ in their ability to ligate human IgG2 and IgG3. Neutrophils homozygous for the FcgammaRIIa-H131 allotype bind more efficiently to IgG3 than the FcgammaRIIa-R131 allotype and are the only human FcgammaR which bind IgG2. Our aim was to determine whether the homozygous FcgammaRIIa-H131 individuals are more susceptible to developing ANCA-associated systemic vasculitis and nephritis due to differential IgG binding and activation. FcgammaRIIa allotype was determined by both allele-specific polymerase chain reaction (PCR) and Southern blotting with allele-specific oligonucleotide probes end-labelled with 32P-gammaATP, after PCR amplification of genomic FcgammaRIIa DNA in 107 Caucasian patients with ANCA+ vasculitis (of whom 89 had renal disease) and 100 ethnically matched controls. Phenotyping of neutrophil FcgammaRIIa alleles was confirmed in some patients by quantitative flow cytometry using murine MoAbs 41H16 and IV.3. Of the patients with ANCA+ systemic vasculitis, 75 had ANCA with specificity for proteinase 3 and 32 with specificity for myeloperoxidase. Overall, no skewing in FcgammaRIIa allotypes was seen in patients compared with controls. No significant increase of the FcgammaRIIa-H131 allotype was found amongst patients irrespective of ANCA specificity, and no association between the FcgammaRIIa allotype and nephritis was found. Our data suggest that the FcgammaRIIa receptor allotype is not a major factor predisposing to the development of ANCA+ systemic vasculitis, or to nephritis. (+info)
Inflammatory cells and cellular activation in the lower respiratory tract in Churg-Strauss syndrome. (4/216)BACKGROUND: To obtain insight into the mechanisms of tissue injury in lung disease due to Churg-Strauss syndrome (CSS), the bronchoalveolar lavage (BAL) cell profile and the levels in the BAL fluid of cell products released by activated eosinophils and neutrophils were assessed. METHODS: Thirteen patients with active progressive CSS (n = 7) or CSS in partial remission (n = 6) underwent clinical staging and bronchoalveolar lavage. The levels of eosinophil cationic protein (ECP), myeloperoxidase (MPO), and peroxidase activity in the BAL fluid were determined and the results were compared with those of 19 patients with pulmonary active Wegener's granulomatosis (WG) and nine control subjects. RESULTS: In patients with progressive CSS the BAL cell profile was dominated by eosinophils, neutrophil elevation being the exception. The eosinophilia was associated with high ECP levels (4.39 ng/ml and 0. 40 ng/ml in the two CSS groups compared with unmeasurable values in the controls). Individual patients with highly active CSS also had raised MPO levels, comparable to the levels in the most active WG patients. Peroxidase activity in the BAL fluid was 1.26 U/ml and 0. 10 U/ml in the two groups of patients with CSS and 0.20 U/ml in the controls. Pulmonary disease in patients with WG was characterised by an extensive increase in MPO (0.30 ng/ml versus 0.13 ng/ml in the controls) together with high peroxidase activity in the BAL fluid (4. 37 U/ml), but only a small increase in ECP levels was seen. No correlation was found between the ECP and MPO levels in patients with CSS which suggests that eosinophil and neutrophil activation vary independently of each other. CONCLUSIONS: These findings suggest that, in addition to eosinophil activation, neutrophil activation is an important feature in some patients with highly active CSS. The balance of neutrophil and eosinophil involvement appears to be variable and this may be one explanation for the individually variable treatment requirements of patients with CSS. (+info)
Disease of the month. The Churg Strauss Syndrome. (5/216)The Churg Strauss Syndrome is an eosinophil-associated small vessel vasculitis. Although its pathogenesis may be distinctive and the association with severe late-onset asthma typical, the clinical features during the vasculitic phase widely overlap with those of the other forms of necrotizing vasculitis, and no single clinical or histologic feature is pathognomic of the condition. Renal involvement is common, although usually mild, and even when severe it tends to respond well to treatment. The prognosis for both patient and renal survival with adequate treatment is in general good. The optimal treatment strategy, however, is uncertain, and may differ from that for the other vasculitides. In particular, in contrast to Wegener's granulomatosis, the need for routine cyclophosphamide treatment is unconfirmed and requires further study. (+info)
Involvement of soluble CD95 in Churg-Strauss syndrome. (6/216)Deficiency of CD95 (Apo-1/Fas)-mediated apoptosis has recently been found in some autoimmune lymphoproliferative disorders due to inherited mutations of the CD95 gene. In this study, impairment of CD95 ligand-mediated killing of lymphocytes and eosinophils in Churg-Strauss Syndrome (CSS), which was a result of variation of CD95 receptor isoform expression, is demonstrated. Compared to those from healthy individuals, peripheral blood lymphocytes from eight CSS patients exhibit a switch from the membrane-bound CD95 receptor expression to its soluble splice variant, which protects from CD95L-mediated apoptosis. In five out of seven CSS patients recurrent oligoclonal T cell expansions were found, all using a Vbeta-gene from the Vbeta21 family associated with similar CDR3 motifs, indicating the predominance of T cell clones of a similar specificity in the CSS patients. In two of them, the effect of immunosuppressive therapy was studied. In both cases aberrant overexpression of the soluble CD95 receptor isoform and deviations from normal TCR Vbeta-gene usage normalized in parallel with the clinical improvement. Furthermore, soluble CD95 was identified as a survival factor for eosinophils rescuing eosinophils from apoptosis in the absence of growth factors in vitro. Given the role of eosinophils as effector cells in CSS, these findings suggest that soluble CD95 may be mechanistically involved in the disease. (+info)
Subclinical alveolar bleeding in pulmonary vasculitides: correlation with indices of disease activity. (7/216)Haemosiderin-laden alveolar macrophages are a common finding in patients with alveolar bleeding. Iron-positive macrophages, suggestive of subclinical alveolar bleeding, were found to be fairly common in bronchoalveolar lavage (BAL) fluid in primary systemic vasculitis but uncommon in collagen vascular diseases (CVDs) and rheumatoid arthritis (RA). To substantiate the impression that subclinical alveolar bleeding may be a feature distinguishing between these disorders, fibreoptic bronchoscopy and BAL were performed in 49 patients with active Wegener's granulomatosis or Churg-Strauss syndrome and 44 patients with CVDs or RA, all of them without clinically manifest alveolar bleeding. The percentage of iron-positive cells was compared with clinical and radiological findings. Only a minority of the CVD and RA patients had iron-positive alveolar macrophages; the 95th percentile of the median number of such cells was 5%. Fifty-three per cent of the patients in the vasculitis group had >5% iron-positive cells, with individual counts ranging up to 95%. Patients with iron-positive macrophages had more extensive disease, more frequent microhaematuria, a higher antineutrophil cytoplasmic antibody titre, a higher myeloperoxidase concentration in the BAL fluid and somewhat more frequent low-attenuation opacities in pulmonary high-resolution computed tomography than the patients with a low iron-positive cell count. In conclusion, subclinical alveolar bleeding was, indeed, a common finding in antineutrophil cytoplasmic antibody-associated vasculitis, which distinguished these disorders from lung disease due to collagen vascular diseases or rheumatoid arthritis. Its association with indices of disease activity, although weak in this cross-sectional study, merits a longitudinal study of its value for the long-term monitoring of vasculitis patients. (+info)
An approach to diagnosis and initial management of systemic vasculitis. (8/216)Systemic vasculitis occurs in a heterogeneous group of primary disorders or can be a manifestation of infection, an adverse drug reaction, malignancy or a connective tissue disease. A vasculitic process should be suspected in patients with unexplained ischemia or multiple organ involvement, especially when such features as polymyalgia rheumatica, inflammatory arthritis, palpable purpura, glomerulonephritis or multiple mononeuropathy are also present. The clinical features of systemic vasculitis depend on the organs involved and, in turn, organ involvement is largely influenced by the size of the affected blood vessels. The diagnostic work-up should be tailored to the clinical situation and geared toward a tissue or angiographic diagnosis, bearing in mind that the findings from these studies are not always pathognomonic. Emphasis should also be placed on exclusion of a secondary process. The diagnosis of the specific type of vasculitis may be made on the basis of the clinical features and the histopathologic or angiographic findings. Initial therapy for most types of systemic vasculitis consists of high-dose corticosteroids, with the addition of immunosuppressive therapy in certain patients. (+info)
The exact cause of Churg-Strauss Syndrome is not known, but it is believed to be related to an abnormal immune response to environmental allergens such as dust mites, pollen, or mold. The symptoms of the condition can vary widely and may include:
1. Respiratory problems: Coughing, wheezing, shortness of breath, and asthma-like symptoms.
2. Skin rashes and lesions: Red, itchy, and inflamed skin rashes, often on the face, arms, and legs.
3. Gastrointestinal problems: Abdominal pain, diarrhea, nausea, and vomiting.
4. Joint pain and swelling: Pain and swelling in the joints, particularly in the hands and feet.
5. Neurological symptoms: Headaches, confusion, seizures, and peripheral neuropathy (nerve damage).
6. Cardiovascular problems: High blood pressure, arrhythmias, and heart failure.
7. Eye problems: Conjunctivitis, uveitis, and blindness.
8. Kidney problems: Proteinuria (excess protein in the urine) and hematuria (blood in the urine).
The diagnosis of Churg-Strauss Syndrome is based on a combination of clinical findings, laboratory tests, and imaging studies. Treatment typically involves corticosteroids, immunosuppressive drugs, and other medications to manage symptoms and reduce inflammation. In severe cases, hospitalization may be required to monitor and treat the patient's condition.
While Churg-Strauss Syndrome is a rare condition, it can have serious consequences if left untreated. Early diagnosis and prompt treatment are essential to prevent complications and improve outcomes for patients with this condition.
There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:
1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.
The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.
Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.
In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:
1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.
It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.
Examples of syndromes include:
1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.
Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.
There are several possible causes of hypereosinophilic syndrome, including:
2. Parasitic infections
3. Autoimmune disorders
5. Genetic conditions
Symptoms of hypereosinophilic syndrome can vary depending on the underlying cause, but may include:
1. Skin rashes or hives
2. Swelling, particularly of the face and lips
3. Difficulty swallowing or breathing
4. Abdominal pain
7. Joint pain
Hypereosinophilic syndrome is diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood counts and biopsies. Treatment depends on the underlying cause of the condition, but may include medications to reduce inflammation and suppress the immune system, as well as antibiotics or anti-parasitic drugs if an infection is suspected. In severe cases, hospitalization may be necessary to monitor and treat the condition.
Prognosis for hypereosinophilic syndrome varies depending on the underlying cause, but with proper treatment, many people with this condition can experience significant improvement in symptoms and quality of life.
There are many possible causes of eosinophilia, including:
* Parasitic infections
* Autoimmune disorders
The symptoms of eosinophilia can vary depending on the underlying cause, but may include:
* Swelling of the skin, lips, and eyes
* Hives or itchy skin
* Shortness of breath or wheezing
* Abdominal pain
Eosinophilia is typically diagnosed through a blood test that measures the number of eosinophils in the blood. Other tests such as imaging studies, skin scrapings, and biopsies may also be used to confirm the diagnosis and identify the underlying cause.
The treatment of eosinophilia depends on the underlying cause, but may include medications such as antihistamines, corticosteroids, and chemotherapy. In some cases, removal of the causative agent or immunomodulatory therapy may be necessary.
Eosinophilia can lead to a number of complications, including:
* Anaphylaxis (a severe allergic reaction)
* Eosinophilic granulomas (collections of eosinophils that can cause organ damage)
* Eosinophilic gastrointestinal disorders (conditions where eosinophils invade the digestive tract)
The prognosis for eosinophilia depends on the underlying cause, but in general, the condition is not life-threatening. However, if left untreated, complications can arise and the condition can have a significant impact on quality of life.
In conclusion, eosinophilia is a condition characterized by an abnormal increase in eosinophils in the body. While it can be caused by a variety of factors, including allergies, infections, and autoimmune disorders, the underlying cause must be identified and treated in order to effectively manage the condition and prevent complications.
The diagnosis of pulmonary eosinophilia is based on a combination of clinical symptoms, physical examination findings, and laboratory tests such as chest X-rays, blood tests, and bronchoalveolar lavage (BAL) fluid analysis.
Treatment of pulmonary eosinophilia depends on the underlying cause and may include medications such as corticosteroids, antihistamines, or antibiotics, as well as lifestyle modifications such as avoiding allergens and managing stress. In severe cases, hospitalization may be necessary to monitor and treat the condition.
Some common symptoms of pulmonary eosinophilia include:
* Shortness of breath (dyspnea)
* Chest tightness or discomfort
* Recurrent respiratory infections
Complications of pulmonary eosinophilia can include:
* Respiratory failure
* Asthma exacerbation
* Chronic obstructive pulmonary disease (COPD)
* Pneumonia or other respiratory infections
* Airway obstruction
It is important to seek medical attention if you experience any of these symptoms, as early diagnosis and treatment can help prevent complications and improve outcomes.
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- CSS has also been shown to be a pathological syndrome of angiitis and allergic granulomatosis . (who.int)
- The disease was known as " Churg-Strauss syndrome ", named after Drs. Jacob Churg and Lotte Strauss who, in 1951, first published about the syndrome using the term " allergic granulomatosis " to describe it. (capsulehealth.one)
- 36. New developments in the treatment of Wegener's granulomatosis, polyarteritis nodosa, microscopic polyangiitis, and Churg-Strauss syndrome. (nih.gov)
- Peripheral neuropathy in Wegener's granulomatosis, Churg-Strauss syndrome and microscopic polyangiitis. (bmj.com)
- Eosinophilic granulomatosis with polyangiitis , also known as Churg-Strauss syndrome, often affects the respiratory tract, gastrointestinal tract, skin, heart and nervous system. (nih.gov)
- Eosinophilic Granulomatosis with Polyangiitis (EGPA), formerly known as Churg-Strauss Syndrome, is a rare condition that can be challenging to diagnose. (player.fm)
- Participants with other conditions that could lead to elevated eosinophils such as hyper-eosinophilic syndromes including (but not limited to) Eosinophilic Granulomatosis with Polyangiitis (EGPA, formerly known as Churg-Strauss Syndrome) or Eosinophilic Esophagitis. (clinicalconnection.com)
- The rare but potentially fatal condition of Allergic Granulomatosis, also named Churg-Strauss Syndrome after the two scientists who discovered it, is generally not recognised or diagnosed until a life-threatening bleed has occurred inside a major organ of the body. (warble.com)
Incidence of Churg-Strauss2
- Although the incidence of Churg-Strauss syndrome associated with zafirlukast therapy is rare, this case report illustrates steps that may be taken to diagnose quickly and treat this life-threatening condition should it occur. (nih.gov)
- Incidence of Churg-Strauss Syndrome is thought to be less than 1 in 100,000. (warble.com)
- EGPA (formerly known as Churg-Strauss syndrome) is a condition characterized by asthma, high levels of eosinophils (a type of white blood cell that helps fight infection), and inflammation of small- to medium-sized blood vessels. (empr.com)
- Churg-Strauss syndrome (CSS) is a rare systemic vasculitis characterized by hypereosinophilia, necrotizing vasculitis with granulomas of extravascular eosinophils and asthma history . (who.int)
- Micrograph showing an eosinophilic vasculitis consistent with Churg-Strauss syndrome. (capsulehealth.one)
- Dr. Robert Lebovics , Site Chair of Otolaryngology and Co-Director of the Airway Center at Mount Sinai West, as well Medical Advisory Board member of the Vasculitis Foundation and Sjogren's Syndrome Foundation, specializes in helping people breathe. (mountsinai.org)
- Most web sites dealing with Churg-Strauss Syndrome do not suggest what the early symptoms may be beyond asthma, I can see, retrospectively, that there were many signs of a worsening vasculitis and greater awareness of such signs may help to save others from developing the syndrome to the point that it threatens their lives. (warble.com)
- One of the American College of Rheumatology criteria for Churg-Strauss syndrome is extravascular eosinophil infiltration on biopsy. (capsulehealth.one)
- Fatal outcome in allopurinol hypersensitivity syndrome]. (nih.gov)
- Neurologic manifestations in primary Sjögren syndrome: a study of 82 patients. (bmj.com)
- Polyarteritis nodosa with lung involvement is called CHURG-STRAUSS SYNDROME. (bvsalud.org)
- For classification purposes, a patient shall be said to have Churg-Strauss syndrome (CSS) if at least 4 of these 6 criteria are positive. (capsulehealth.one)
- In this report, a case is described of a 47-year-old white man with moderate persistent asthma in whom Churg-Strauss syndrome developed while he was receiving zafirlukast therapy. (nih.gov)
- It seems that nobody is entirely sure what causes Churg-Strauss but a favourite theory is that a dependence on steroids may be partly to blame, and a group of people who seem particularly at risk from the disease are asthma sufferers, who tend to take inhalers containing steroids on a frequent basis. (warble.com)
- Some studies have shown that asthma sufferers have often developed Churg-Strauss shortly after changing their inhalers, this raised questions over whether or not the new inhalers were causing the disease but further research suggested it was more likely to be the cessation of using the previous steroidal inhaler that was bringing Churg-Strauss to the fore. (warble.com)
- Inhaler changes tend to be made following bad asthma attacks, therefore bad asthma attacks are often part of the recent history of a Churg-Strauss sufferer. (warble.com)
- It is also however widely thought that Churg-Strauss can cause asthma or asthma-like symptoms, so an apparent worsening of asthma may well be caused by Churg-Strauss itself, and if, in those rare cases, the steroidal inhalers are not working well then the change to a non-steroidal inhaler is likely to make the Churg-Strauss much worse. (warble.com)
- Perhaps paradoxically, Ladan found that her new non-steroidal inhaler worked wonders for her asthma, which perhaps suggests that it is the asthma that was worse rather than Churg-Strauss causing it. (warble.com)
- Most of what I am about to write is based on what were, with retrospective vision, probably symptoms of Churg-Strauss, in the hope that if you have found this article by searching for symptoms in a search engine, and the picture seems to fit your case, you might ask for an ANCA test to be taken as a precaution. (warble.com)
Long QT Syndr1
- Potential areas of application could include but are not limited to the following: o Heart and Vascular Diseases: arrhythmogenic right ventricular dysplasia, Brugada's Syndrome, congenital heart disease, familial homozygous hypercholesterolemia, Liddle's Syndrome, Long QT Syndrome. (nih.gov)
- o Sleep Disorders: congenital central hypoventilation syndrome (Ondine's Curse), circadian rhythm disorders such as advanced sleep phase syndrome. (nih.gov)
- Cogan's syndrome is an autoimmune disorder that mainly affects the eyes and inner ears along with large blood vessels. (nih.gov)
- The primary method of diagnosing Churg-Strauss is not however from the deadly bleed itself, but rather through the results of a particular blood test called ANCA (anti-neutrophilic cytoplasmic antibodies). (warble.com)
- Severe rash or swelling, such as Stevens-Johnson syndrome . (medicalnewstoday.com)
- Withdrawal syndrome in 2 drug addicts after intravenous injection of buprenorphine? (bvsalud.org)
- Arteritis involving large, medium sized, and small arteries, and associated with mucocutaneous lymph node syndrome. (bmj.com)
- Churg-Strauss syndrome (CSS) is a systemic inflammatory disease characterized by asthma, eosinophilia, and involvement of various organ systems such as the upper and lower respiratory tract, the peripheral nervous system, the skin, the kidney and the gastrointestinal tract. (medscape.com)
- Keogh KA, Specks U. Churg-Strauss syndrome: clinical presentation, antineutrophil cytoplasmic antibodies, and leukotriene receptor antagonists. (medscape.com)
- Churg-Strauss syndrome in patients receiving montelukast as treatment for asthma. (medscape.com)